Evidence map›Paper›PMID 39519266›Full record

ArticleInternational journal of molecular sciences2024

Autocrine Motility Factor and Its Peptide Derivative Inhibit Triple-Negative Breast Cancer by Regulating Wound Repair, Survival, and Drug Efflux.

Se Gie Kim, Seok Joong Kim, Thanh Van Duong, Yuhan Cho, Bogeun Park, Ulhas Sopanrao Kadam, Hee Sung Park, Jong Chan Hong

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Se Gie KimDepartment of Cosmetic Science, Kyungsung University, Busan 48434, Republic of Korea.
Seok Joong KimDepartment of Food and Nutrition, College of Natural and Information Science, Dongduk Women's University, Seoul 02758, Republic of Korea.
Thanh Van DuongDepartment of Anatomy, School of Medicine, Pusan National University, Yangsan 50612, Republic of Korea.
Yuhan ChoDivision of Applied Life Science (BK21 Four), Plant Molecular Biology and Biotechnology Research Center, Gyeongsang National University, Jinju 52828, Republic of Korea.
Bogeun ParkDivision of Applied Life Science (BK21 Four), Plant Molecular Biology and Biotechnology Research Center, Gyeongsang National University, Jinju 52828, Republic of Korea.
Ulhas Sopanrao KadamDivision of Applied Life Science (BK21 Four), Plant Molecular Biology and Biotechnology Research Center, Gyeongsang National University, Jinju 52828, Republic of Korea.ORCID 0000-0001-8737-167X
Hee Sung ParkDivision of Applied Life Science (BK21 Four), Plant Molecular Biology and Biotechnology Research Center, Gyeongsang National University, Jinju 52828, Republic of Korea.ORCID 0000-0002-3415-9197
Jong Chan HongDivision of Applied Life Science (BK21 Four), Plant Molecular Biology and Biotechnology Research Center, Gyeongsang National University, Jinju 52828, Republic of Korea.

Funding

Ministry of Education 2020R1F1A1074027Ministry of Education 2022R1I1A1A01063465
6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) presents a significant challenge in oncology due to its aggressive nature and limited targeted therapeutic options. This study explores the potential of autocrine motility factor (AMF) and an AMF-derived peptide as novel treatments for TNBC. AMF, primarily secreted by neoplastic cells, plays a crucial role in cancer cell motility, metastasis, and proliferation. The research demonstrates that AMF and its derived peptide inhibit TNBC cell proliferation by modulating cellular migration, redox homeostasis, apoptotic pathways, and drug efflux mechanisms. Dose-dependent antiproliferative effects were observed across three TNBC cell lines, with higher concentrations impairing cellular migration. Mechanistic studies revealed decreased glucose-6-phosphate dehydrogenase expression and elevated reactive oxygen species production, suggesting redox imbalance as a primary mediator of apoptosis. Combination studies with conventional therapeutics showed near-complete eradication of resistant TNBC cells. The observed reduction in p53 levels and increased intranuclear doxorubicin accumulation highlight the AMF/AMF peptide's potential as multidrug resistance modulators. This study underscores the promise of using AMF/AMF peptide as a novel therapeutic approach for TNBC, addressing current treatment limitations and warranting further investigation.

Indexed as

ApoptosisCell MovementCell ProliferationTriple Negative Breast NeoplasmsWound HealingAntineoplastic AgentsCell Line, TumorCell SurvivalDoxorubicinDrug Resistance, NeoplasmFemaleHumansPeptidesReactive Oxygen SpeciesAntineoplastic AgentsDoxorubicinPeptidesReactive Oxygen Speciesapoptosisautocrine motility factordrug accumulationresistancetriple-negative breast cancer

Identifiers

PMID39519266
PMCPMC11546756

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.